The regulatory role of retinoids in growth and differentiation has been examined in vitro and in vivo by light and scanning electron microscopy using retinoid-deficient and control quail embryos between the 6-15 somite stage, as well as 2- and 2.5-day-old embryos. Retinoid deprivation during embryonal development causes abnormalities in organs of epithelial and mesenchymal origin, most dramatically preventing the formation of the extraembryonal circulatory system. Initial observations with early quail blastodermis incubated in vivo or cultured in vitro suggested that the earliest observable developmental defects in the retinoid-deficient embryo were localized in the heart region. Light microscopic and SEM studies indicate that in the deficient embryo the following sequences of events lead to vascular abnormalities: 1) if development of the heart is retarded before fusion of the two primitive endothelial heart tubes takes place, i.e., prior to the 7-somite stage, a cardia bifida forms; 2) if retardation manifests itself sometime later, a single enlarged ventricle develops in situ verso. Heart development is known to proceed in anteroposterior direction, and the impact of retinoid deficiency was found to be most severe in the posterior region. Since during development the pacemaker region that regulates heart function is always located in the most posterior region of the heart, growth retardation in that area due to retinoid deficiency also resulted in severe reduction of heart beats. In all cases, the omphalomesenteric veins that normally extend caudad from the sinus venosus are not developed and the endocardium of the heart terminates as a blind pouch in the mid-ventral region of the animal. The results thus provide evidence for the failure to establish, at the level of the omphalomesenteric veins, a connection between the embryonal and extraembryonal circulatory system in the retinoid-deficient quail embryos.